Abstract

Effects of chronic and massive amounts of α-bungarotoxin introduced into the yolk sac of the duck embryo on the magnitude of the spontaneously occurring embryonic cell death in the trochlear nucleus were examined. As expected, the embryos continuously treated with the toxin remained paralyzed. As long as the embryos remained continously paralyzed during the period of normal cell death, a significant increase in the number of trochlear neurons occurred. Axon counts of the trochlear nerve indicated a corresponding increase in the number of nerve fibers. Counts of the myelinated and unmyelinated fibers indicated that the increased fiber count was primarily due to increased numbers of unmyelinated axons. Because the increased cell number is due neither to a stimulatory effect of the toxin on cellular proliferation nor to a transient effect, this increase is interpreted to mean a reduction in the magnitude of the embryonic cell death. As revealed by the retrograde axonal flow of horseradish peroxidase, all trochlear neurons including those which had been prevented from dying during the period of paralysis projected to their appropriate peripheral muscle suggesting that they did not survive by virtue of making improper connections. When the toxin treatment was carried out only during the period of cell death and subsequently discontinued, the embryonic motility increased. Cells which were prevented from dying during the period of paralysis degenerated. Counts of the myelinated and unmyelinated fibers indicated a corresponding loss of nerve fibers and that loss of both classes of fibers occurred.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call